Glucose modulation of postganglionic sympathetic neurons innervating blood vessels

Abstract

The present study tested the hypothesis that elevated glucose modulates postganglionic sympathetic neurons innervating blood vessels by studying effects of hyperglycemia on norepinephrine (NE) synthesis (tyrosine hydroxylase (TH)), NE release, and NE uptake (NE transporter (NET)). Effects were studied in vivo in rats made hyperglycemic (313+ 18.3 mg/dl) with STZ (50 mg/kg). In this model, elevated glucose increased TH (western analysis) in postganglionic sympathetic neurons innervating tail arteries (n = 5). Elevated glucose also increased basal NE release (tritiated‐NE released/tritiated‐NE taken up) from isolated rat tail arteries. NE released in 25 mM glucose (4.0+1.02%) was greater than that released in 5 mM glucose (1.78+0.15%; n = 4; p < 0.05). Hyperglycemia also modulated cultured postganglionic sympathetic neurons. NET (western analysis) in neurons grown in 25 mM glucose was markedly increased compared to that in neurons grown in 5 mM glucose (n = 3). These data clearly indicate that elevated glucose affects the function of postganglionic sympathetic neurons innervating blood vessels. The in vitro data suggest that glucose directly affects postganglionic sympathetic neurons, suggesting that sympathetic ganglia are more than passive relays. These findings may have important implications for sympathetic control of cardiovascular function under hyperglycemic conditions. HL076774, NS043316